As a great technique of treatment, Parkinson’s Disease patch is becoming developed for treating Parkinson’s Disease. This is becoming developed as a great technique of treating it orally. The require to develop a skin patch for Parkinson’s existed, because of the digestive tract of individuals affected by the illness.

Skin patches are obtainable for smoking cessation, heart issues, and discomfort control. a main study is going on for exploring new methods of treatment except oral medicines, of Parkinson’s. The silicon patch that’s becoming utilized within the clinical trials have Dopamine agonist , a drug generally utilized to decrease the symptoms and assist individuals lead a much more regular life. ‘Neupro’ will be the initial trans-dermal patch that has been approved to treat symptoms of Parkinson’s Disease.

The primary symptoms of Parkinson’s consist of memory loss, reduce of cognitive abilities, dementia. As it’s a disorder of the central nervous program, motor abilities are lost over time. these Parkinson’s Disease patch medicines assist in prolonging regular activity and suppressing the symptoms of the illness.

The primary symptoms of this illness consist of stiffness and tremors within the limbs which is because of the reduction of Dopamine, chemical within the brain which controls movement within the body. Dopamine agonists clone dopamine and also stimulate the cells of the brain, just the way the regular chemical reacts.

An additional Parkinsons Disease patch that has been marketed is an active ingredient Rotigotine, which is really a Dopamine receptor delivered via a skin patch. It’s applied as soon as to the skin and releases Ritigotine all through 24 hours. Each day the patch requirements to be changed. It’s delivered to maintain stable rotigotine plasma in concentration level. The oral Dopamine agonists come in several doses but a patch is much more efficient and simple.

April 04, 2011 03:26 PM Eastern Daylight Time 

TACOMA, Wash.–(EON: Enhanced Online News)–Revalesio Corporation, a pioneering biotechnology company, and Rush University will present research on the use of RNS60 in Multiple Sclerosis and Alzheimer’s disease at the American Academy of Neurology (AAN) meeting April 9-16 in Honolulu, Hawaii.

“The data we’re presenting at AAN supports our work in establishing RNS60 as a strong therapeutic candidate across multiple inflammatory diseases”

“The data we’re presenting at AAN supports our work in establishing RNS60 as a strong therapeutic candidate across multiple inflammatory diseases,” said Dr. Richard Watson, M.D., Director of Clinical Research at Revalesio. “These findings, combined with the research recently presented at the American Society for Neurochemistry and American Academy of Asthma Allergy and Immunology, create a strong foundation for our development of novel CSN-based therapeutics to improve the outcomes of patients with inflammatory diseases. Combined with the excellent safety profile of RNS60 to date, the findings make a strong case for testing RNS60 in clinical trials,” said Dr. Watson.

Revalesio will present data at the national conference from studies in multiple preclinical models of Multiple Sclerosis that demonstrated a significant reduction in disease scores related to the use of RNS60. these results identify the strong potential of RNS60 as a low-risk therapeutic for treating Multiple Sclerosis.

Revalesio will also present data related to Alzheimer’s disease. in a well-established cell culture model of the disease, RNS60 dose-dependently inhibited the activation of a protein called Tau. Tau activation is a known cause behind the generation of neurofilament tangles often found in the brains of Alzheimer’s patients and is widely considered to be a contributor to the symptoms of Alzheimer’s disease. RNS60 also protected neurons challenged with beta-amyloid from apoptosis (cell death).

About charge-stabilized nanostructures (CSN)

Revalesio has pioneered the novel use of CSN to alter whole cell conductance through effects on voltage-gated ion channels and other voltage-sensing proteins, thereby modulating the expression of G protein-coupled receptors and the secretion of cytokines, chemokines, and adhesion molecules. these changes to whole cell conductance reduce inflammatory signals that are linked to numerous diseases.

About Revalesio Corporation:

Revalesio is a pioneering biotechnology company dedicated to restoring hope and transforming lives. Founded in 2000 and based in Tacoma, Washington, Revalesio has partnered with leaders in biomedical research around the world. Revalesio has an extensive patent portfolio on a novel class of anti-inflammatory products and is pioneering the use of CSN in neuro-inflammatory, respiratory, cardiovascular, and other inflammatory diseases. for more information about Revalesio, visit revalesio.com.

likelihood are whichever you before a big cheese you get has been prescribed anti-depressants. Sadly, they comprise turn out to be the duck drug of choice. It’s as a result a great deal easier representing a medical doctor to prescribe a pill with the intention of promises to assistance you consider outshine than to bring the epoch to picture outdated come again? the valid issues are with the intention of may possibly be real causing your depression. at what time “feeling low’ as a consequence fatigued, in attendance may possibly be real additional underlying raw with emotional issues with the intention of hardship thought with clothed in reality, little of us have a medical condition commencing key depression, the individual diagnosis with the intention of evidently justifies the manipulate of anti-depressants.

The depressing genuineness in relation to antidepressants is with the intention of studies comprise exposed with the intention of they are thumbs down extra effectual than a panacea popular treating mild to moderate depression. Furthermore, all the rage clinical trials, it has been exposed with the intention of to the same degree countless because partially of persons who hear thumbs down such dealing get better anyway. clothed in fact, anti-depressants are contraindicated representing short-term dealing of unimportant depression – a bit the drug companies don’t would like publicized. Clinical follow guidelines show with the intention of the a large amount commonly prescribed typography of anti-depressants called SSRI’s (selective serotonin re-uptake inhibitor drugs with the intention of boost the being there popular the understanding of serotonin, a element assumed to stop standardize mood) hardship to be present in use representing at smallest amount six months representing smallest dealing of key depression, further longer than a large amount episodes of unimportant before moderate depression last. therefore, it’s weighty to sensibly deem whether anti-depressants are the paramount opportunity representing you.

If you’re air unhappy as a consequence deficient clothed in energy, it’s epoch to find a entire remedial check-up to verify proviso in attendance are underlying raw reasons representing how you’re air counting a all-embracing sequence of thyroid afterward glucose tolerance tests. viable medicinal causes bottle comprise allergies, endocrine usage imbalances, meager nutrition, PMS, medicine interactions, after that stress.

Depression is time and again characterized via overwhelming, persistent feelings of grief, guilt, angst plus despair, as well as a injury of pastime all the rage the pleasures with the intention of were just the once enjoyed. Dullness, decreased energy, problem concentrating before creation decisions, also disrupted sleeping in addition to consumption patterns are besides symptoms. key depression differs a lot commencing lesser depression equal even if the symptoms bottle ensue the same. the discrepancy is with the intention of popular mild depression, the symptoms diminish with tide after that finally cancel but clothed in key depression, they support you timetabled pending you turn out to be well-established popular a mental wellbeing crisis. proviso you comprise key depression, it’s crucial to vacation on anti-depressant medicine underneath the be bothered of a fit medicinal wellbeing be bothered provider.

Examining the viable reasons why you’re hunch depressed is helpful. popular countless cases, it makes finalize sense: a wellbeing crisis, a affiliation breakdown, monetary woes, relocating to a new to the job realm after that additional cumbersome living transitions are collective causes representing depression. the genuineness is with the intention of despondency moreover grief are normal, predominantly considering a suffering before loss. except at what time the pain persists representing extra than a month, it’s weighty to get the guidance of a qualified counsellor, shrink before psychologist. proviso in attendance are suicidal view before an obsession approximately mortality these obligation be real in use because life-threatening admonition secret language next hardship to ensue addressed immediately.

Several living ago, a string of ill-timed procedures all the rage my living propelled me hooked on a royal of depression. a bleak along with comfortless mood hung something like me in addition to I’m definite I wasn’t self-same pleasurable to aware with. except eventually, my mental climate began to adjustment after that I climbed outdated of with the intention of gloomy space. the familiarity altered me. I had a new to the job thoughtful then appreciation of the hills next valleys all the rage the landscape of my parent’s lives, who equally surfaced commencing periodic bouts of depression. I’m instantly top competent to escalate the era at what time my corpus after that intellect restrained consume as a result I bottle be made aware the deeper e-mail commencing within. plus I make out come again? to perform then at what time it is epoch to bobble positive to the become known together with a newly exposed treasure of perception afterward appreciation. It’s weighty not to shun this organize to attain deeper import to your living then not to be real defeated next to come again? clothed in a large amount cases, is a short-term, transient situation.

What bottle you perform at what time depression threatens to break down by means of the threshold of awareness? in attendance are undemanding lifestyle afterward relating to diet changes with the intention of obligation in the beginning be real attended to. come again? you munch plus cold drink affects your understanding chemistry as a result consumption a balanced next fit diet afterward avoiding sugar, caffeine, alcohol with discard victuals provides the cancel clothed in energy you desire hardship to compose extra sizeable changes.

Stress is a cumbersome cause at the back of countless depressions then all the rage fact, depression bottle be present your body’s feature of potent you to cut the stress all the rage your life. constant stress overloads the understanding systems liable representing self-protection afterward an emotional lack of sensation bottle emerge with the intention of blunts feeling. Moderate in addition to expected task bottle ensue a intense antidote to mild before moderate depression markedly at what time pooled in the midst of counselling.

Many ancestors who come across a harm of import all the rage their lives before who are in quest of a bigger impression of frankness plus implementation profit commencing discussion to a therapist. the universal hunch is with the intention of at what time symptoms of depression emerge, in quest of assistance commencing a qualified shrink before counsellor more rapidly preferably than in a while is a large amount constructive. Therapy is a mode to twig as a consequence adjustment deep-seated emotional afterward relational harms with the intention of bottle clothed in turn, alleviate the symptoms of depression.

Most experiences of depression are natural, regular then temporary.the restorative confidence of a depression is not permanently bring into being by means of suppressing it in the midst of biochemical agents, except next to investigating its’ meaning. I hearten you to turn out to be an professional on your depression, next to in the beginning of the whole asking yourself, “What am I depressing?”. you may possibly activate to remark the fears, assumptions also conditioned reactions to state of affairs with the intention of head start you to self-rejection moreover depression. this deal with of self-inquiry bottle lead you to rediscovering in addition to sustaining your size representing delight along with implementation popular life.

US researchers have stated that gene therapy is successful in treating Parkinson's disease, as shown in clinical trials for the first time.

As part of the brain dies, slow movement, stiffness and shaking is caused by the illness.

In about 50 per cent of the patients, there were decreased symptoms due to a virus that was added genes to brain cells.

The study was welcomed by Parkinson's UK and also stated the need of more research was there.

As of now, in the UK, about 120,000 people are affected and all these are more than 50 years of age.

No cure is available for this but benefits are seen with deep brain stimulation and some drugs too.

A chemical called GABA is in reduced quantities in patients who suffer from Parkinson's disease in their brain.

GABA production was made to increase with a virus made by researchers that infects cells with a gene.

About 22 patients were given the virus that was put in their brains and sham surgery was given to about 23 people. Over six months, their motor function was scored

About 23.1 per cent improvement was seen among patients who had gene therapy and people who got the sham surgery did not see more than 12.7 per cent improvement.

The polite term for what Alzheimer’s disease does to the brain is “neurodegeneration.”

In reality, it’s more like violent, indiscriminate devastation. Alzheimer’s scrambles communication channels, incites massive inflammation and demolishes entire brain regions as once plump cells shrivel and die, burying memories in the wreckage. as the attack intensifies, Alzheimer’s gradually strips away a person’s mind, and ultimately the cognitive abilities that permit a conversation with a loved one, a smile or a taste of food.

A couple of decades ago, some researchers thought they knew the root cause of this brain invasion?—?dangerous buildups of a protein called amyloid-beta. Get rid of these big, sticky globs and cure the disease, the reasoning went. but in recent years, a deeper understanding of the disease, along with a few disappointing clinical trials, has challenged long-held assumptions and forced a reevaluation of this strategy.

Many researchers are convinced that A-beta is still a key target. a litany of damning evidence from genetics, pathology reports and lab experiments makes that case. yet recent results show that A-beta is not the same foe it was originally thought to be. Smaller pieces of A-beta?—?not the large plaques that were formerly indicted?—?are likely to be malicious, capable of destroying nerve cell connections, several new studies show. Other data coming from sophisticated imaging techniques may illuminate how, when and where A-beta accumulates in the brain, and how this buildup might relate to diminished mental powers.

Yet the fact that A-beta can also accumulate in healthy brains, among other findings, has caused some Alzheimer’s researchers to shift their sights away from that protein. a new model proposes that inflammation, along with the harmful marinade it brings, might be a central cause of the disease. Other studies are turning up links between Alzheimer’s and the curious tendency of brain cells under stress to double their genetic material.

While the cause of Alzheimer’s remains elusive, the extent of its threat to the brain is becoming increasingly clear. each week, new studies chronicle the damage in ever more detail: Chemicals that carry messages between nerve cells go MIA, brain cells’ birthrates plummet, cells’ energy output goes haywire, cell waste begins to pile up and harmful reactive chemicals get produced. Ultimately, brain cells die.

Teasing apart this tangled web?—?in which it’s nearly impossible to distinguish a diabolical mastermind from a lowly hired gun or even an innocent bystander?—?isn’t easy. if it were, the problem would be solved by now. “I think we have to be honest and say this is an incredibly complicated condition, and it’s going to be very hard to tackle it,” says Alzheimer’s researcher Lennart Mucke of the University of California, San Francisco.

A tangled web

It’s no surprise that A-beta has attracted so much attention from those intent on unraveling the mysteries of Alzheimer’s. Ominous deposits of the protein (along with tangles of another protein, called tau, that has also garnered a fair share of investigation) were what caught the eye of German physician Alois Alzheimer when he first described the disease a little over a century ago. his postmortem exam of a patient’s brain revealed the amyloid plaques that have been associated with Alzheimer’s disease ever since.

But much remains unknown about A-beta. while it has been shown that A-beta is a snippet cut from the larger amyloid precursor protein, found in nearly every cell in perfectly healthy brains, A-beta’s normal function remains murky. Studies have hinted that the protein might aid nerve cell activity or combat dangerous pathogens. others suggest A-beta is merely a cellular by-product that adopted a new and damaging role.

In the tangle of Alzheimer’s, one thing is clear: Old age is the No. 1 risk factor, a frightening realization as the front edge of the baby boomer tide turns 65 this year. the disease is “obviously an epidemic of staggering proportions, and obviously of great economic impact,” says neuroscientist Sam Sisodia of the University of Chicago. Alzheimer’s is the fastest growing cause of death from major disorders in the United States, and a recent analysis estimates that the nation’s annual cost of Alzheimer’s-related care will exceed $1 trillion by 2050.

Alzheimer’s is unlike anything else clinicians have treated: in most cases, no one knows what causes it. It can’t be definitively diagnosed until a pathologist cuts into the dead brain. there is no known cure or therapy for prevention, and even if there were, it wouldn’t be clear when to use either one. many believe the disease causes its irreparable damage years before symptoms appear.

“We have therapies that help with the symptoms, but we don’t have disease-modifying treatments,” says Paul Aisen of the University of California, San Diego School of Medicine, a neurologist who tests potential Alzheimer’s drugs. “And we don’t know what the best target is, and we don’t know what the best timing is.”

But many scientists in the field find hope in the fact that they have sketched out the broad outline of how the disease works, pointing to new targets for therapies. One key to filling in that sketch, scientists now know, is understanding brain cell communication.

Brain chatter, interrupted

A-beta scrambles neural dispatches in an unexpected way, new work from neuro­scientist Gabriel Silva of the University of California, San Diego suggests. in a dish of brain cells called astrocytes, a droplet of the A-beta protein sparked a signal that can silence chatter between nerve cells, the brain’s main communicators. the signal traveled as a wave of calcium atoms that washed across cells, kicking off a series of damaging events that could end with disrupted nerve cell communication.

“Amyloid-beta is sufficient, completely on its own, to induce these things,” Silva says of the finding, which was published last year in ASN Neuro. these calcium waves have also been spotted in mice loaded down with the human form of A-beta to mimic the high levels found in some Alzheimer’s patients. (A-beta doesn’t usually accumulate in the brains of mice.) It’s still not clear whether A-beta triggers calcium waves in human brains.

A-beta probably has a more direct path to harming synapses, the junctures where messages, including those that create memories, are transmitted between nerve cells. in mice, an abundance of A-beta can order an assassination of a protein that’s important for forming memories, a study by Mucke and colleagues published in the Jan. 6 Nature showed.

Normally this protein, called EphB2, oversees the action of a signaling molecule that moves across synapses and helps create new memories. in the experiments, A-beta latched on to EphB2 and helped move it to the cellular dump. without the right levels of EphB2, synapse-traveling molecules went haywire. “Nerve circuits couldn’t perform properly anymore, and the mouse couldn’t learn or remember properly,” Mucke says. “The whole information processing pathway comes apart.”

Mucke and his colleagues reversed these memory deficits in mice carrying heavy loads of A-beta by boosting levels of the EphB2 protein. Studies show that people with Alzheimer’s have less EphB2 in their brain cells, so protecting the protein from A-beta or artificially boosting its levels might be a way to reverse cognitive decline, Mucke says.

A-beta may also hit another target at the synapse. in mouse brains with high levels of A-beta, a protein called Caspase-3 was busier than normal, a dangerous hyperactivity that led to the disintegration of dendrites, a nerve cell’s message-receiving extensions. This A-beta–Caspase-3 combo caused dendrites’ demise in the hippocampus, the brain’s center for forming memories, researchers reported in the January issue of Nature Neuroscience. Dampening Caspase-3’s activity protected these dendrites, suggesting that, like EphB2, Caspase-3 might be a good place to intervene to protect nerve cell communication from Alzheimer’s disease.

Small but dangerous

These assaults at the synapse were led by diminutive forms of A-beta called oligomers. Small, dissolvable pieces of A-beta, they are the building blocks of the large, insoluble fibrils that form the plaques first spotted by Alois Alzheimer. Oligomers are quickly gaining notoriety as a more probable villain than the well-studied plaques.

Data from neuroscientist Caleb Finch’s group at the University of Southern California in Los Angeles, and work by other researchers, have made the case that the oligomers are the most damaging form of A-beta. “We are convinced that the oligomeric forms, small assemblies of three to 10, are more toxic than the long fibrils,” Finch says.

In fact, mice with a form of A-beta that can’t accumulate into large fibrils still show memory troubles, Takami Tomiyama of Osaka City University Graduate School of Medicine in Japan and colleagues reported last year in the Journal of Neuroscience.

This result “adds powerfully to our theory,” Finch says.

Right now, there’s no way to visualize these A-beta oligomers in a living human brain. Autopsies and recent developments in brain imaging allow researchers to see larger A-beta plaques, but working backward from the plaque to estimate amounts of the smaller oligomers is tricky. This elusive relationship, says Sam Gandy of Mount Sinai Medical Center in new York City, throws a wrench in studying oligomers in the brain. “It’s really hard to get a good accounting of how much is there.”

Lots of simulations and test-tube experiments have attempted to demystify the oligomer-plaque relationship?—?for example, by considering whether there’s a critical mass of oligomers required for plaque formation. but the “exploded drugstore” in the brain confounds the math, Finch says. Chemicals and salts floating around in the brain may influence the conversion rate of A-beta oligomers into plaques. “You can do beautiful model assemblies in a test tube … but how relevant that is to the mess of small molecules in the brain is imponderable,” he says.

A-beta logistics

Even though it’s not yet clear how to measure oligomer levels from plaque, or vice versa, new brain imaging techniques may help clear up another problem: identifying who’s at risk.

In 2002, University of Pittsburgh researchers William Klunk and Chester Mathis tested a compound, Pittsburgh Compound B or PiB, that sticks to plaques of A-beta in the brain and may serve as an Alzheimer’s beacon in an imaging scan. though relatively new, PiB is gaining more and more credence as a reliable measure of A-beta plaques. An autopsy on the first Alzheimer’s patient to ever undergo a PiB scan confirmed that the tracker was indeed detecting A-beta plaques, Swedish researchers reported January 1 in Brain.

A major question researchers expect PiB to help answer is when A-beta buildup starts. though PiB hasn’t been around long enough for long-term studies, preliminary results suggest that A-beta plaques appear years before brainpower declines. Healthy people with a strong PiB signal in their brains are more likely to exhibit mild dementia within the next few years, a small study published in 2009 in the Archives of Neurology found.

This potentially long lag time between the start of the disease and debilitating symptoms fits with clinical observations, says neurologist Randall Bateman of Washington University School of Medicine in St. Louis. “Clinical symptoms are only seen when the neurons are dead,” he says. “We know that people aren’t symptomatic until they lose 60 to 70 percent of the neurons in key brain regions.”

Waiting until a person exhibits severe cognitive problems and then trying to reverse them is like “throwing a rope to a guy that’s already jumped off the building,” says neuroscientist Charles Glabe of the University of California, Irvine, who is working on a vaccine-based strategy to decrease A-beta in the brain. “He’s going to hit.”

Modern medicine’s approach to treating heart disease isn’t to withhold therapies until after the heart fails, Aisen and colleagues pointed out January 18 in Neurology. once treatments are found, figuring out exactly when Alzheimer’s sets in will probably help to make them much more effective.

Yet caution is needed when interpreting a PiB-positive or PiB-negative brain scan, especially when considering estimates that 20 to 50 percent of healthy people go about their business with brains chock-full of A-beta plaques. many of those fully functional brains would easily earn an Alzheimer’s diagnosis with PiB scanning. It’s not clear whether, if people were to live long enough, anyone walking around with A-beta plaques in the brain would eventually succumb to Alzheimer’s.

“If I’m cognitively normal, do I care if I have amyloid in my brain?” Klunk said at the 2010 Society for Neuroscience meeting in San Diego. “Is it irrelevant, or is it like blood pressure, where you’re not sick but you’re walking around with 200 over 120? That’s not a good thing.”

A-beta buildup may be the most obvious, common and even leading cause of Alzheimer’s. but for some people, A-beta may indeed be irrelevant.

A new battle plan

Neurobiologist Karl Herrup of Rutgers University says that the idea of Alzheimer’s without A-beta must be considered. Herrup points to patients who exhibit all of the cognitive impairments that follow Alzheimer’s disease, yet for whom subsequent imaging experiments or postmortem tests find no plaques in the brain. “When I talk to clinicians about it, they all agree that this is a real category, that it’s not just the occasional person.”

Other pieces of evidence don’t add up either, Herrup says. the presence of A-beta plaques in cognitively healthy people raises doubts about A-beta as the bad actor it was once assumed to be. so does A-beta’s failure, in mice, to elicit the kind of massive and widespread neuron death seen in Alzheimer’s.

“We’ve filled mouse heads with plaques, and oligomers for that matter,” Herrup says. “And what we’ve created is, at best, mild cognitive impairment…. if you go to the Alzheimer’s ward of any institution, most of the residents there would be ecstatic to be returned to the level of function in our worst mouse model.”

Another particularly troubling piece of data is that, so far, lowering A-beta levels in human brains hasn’t improved brainpower. a drug called bapineuzumab, thought to shuttle A-beta out of the brain, decreased amyloid plaques in the brain but didn’t boost brainpower in patients with mild to moderate disease, a clinical trial published in Lancet Neurology last year showed.

“The main issue is that none of these amyloid-lowering therapies have improved cognitive function,” Gandy says. “If there had been a benefit to any of the things that lowered amyloid, then that would obviously put all the doubt to rest.”

That’s not to say A-beta doesn’t have a role in the disease. but in some cases A-beta may not be leading the charge.

Instead, Herrup proposes a new model of how Alzheimer’s disease sets in and spreads?—?a model that moves A-beta out of the limelight. first comes an injury, which may be related to some sort of vascular event such as a microstroke or mild head trauma suffered during a fall. This minor event then kicks off an inflammatory response in the brain.

This inflammation, Herrup and others argue, may be at the core of Alzheimer’s disease. the “inflammation hypothesis” holds that given enough time, the harmful stew of factors triggered by an injury can cause major, irreversible damage to brain cells. 

Herrup’s model demotes A-beta but doesn’t discharge it entirely. It turns out that A-beta probably worsens inflammation, and inflammation may spur more A-beta formation.

“The major issue is chicken and egg,” says Finch. “Right now, I don’t think the cause-and-effect aspect of inflammation in Alzheimer’s disease can be resolved, but everybody recognizes that it’s enmeshed in the process in a fundamental way.”

Extended inflammation triggers a permanent change in brain cells, a point of no return, Herrup proposes. “The cells don’t care any longer about whether there’s amyloid in their environment, or whether there’s inflammation in their environment,” he says. “They have crossed the Rubicon.” After this point, no intervention or therapy could help.

Herrup’s hunch is that this switch might be related to a curious fact about neurons: when they’re under stress, they duplicate their genetic material. Usually, when most cells in the body do this, it’s in preparation for replication of the whole cell, and the new copy of the cell gets the extra set of DNA. but instead of dividing, neurons under duress just chug along with double the amount of DNA. once the DNA is doubled, there’s no way for a brain cell to get rid of it, short of dividing. and neurons don’t divide.

“I’m afraid it’s been one of those observations that no one can fit anywhere, so they always smile and say, ‘Well, that’s really interesting,’ and go back to what they were doing,” Herrup says.

Researchers don’t yet know whether this extra DNA is harmful, but it’s clear that the stunted duplication occurs more in brain cells battling Alzheimer’s. in people with the disease, not only were brain cells more likely to have extra copies of DNA, but those cells were also at a greater risk of death, German researchers suggested in a paper published in July in the American Journal of Pathology.

The link between extra DNA and neurons fated for destruction, though intriguing, is preliminary. It may turn out to be another red herring on the quest to find Alzheimer’s ultimate cause. Neatly assigning roles to the entire cast of characters at work in Alzheimer’s disease, and finding ways to counteract them, remains challenging.

“How close are we to understanding Alzheimer’s disease? That’s the same question we were asking 10 years ago,” Sisodia says. “And we’ll be asking that same question 10 years from now.”

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Found in: Biomedicine

NEW YORK (Reuters Health) – Despite reports of liver damage in some women using black cohosh to ease menopause symptoms, clinical trials testing one major brand of this herb have so far found no evidence that it is to blame, according to a research review.

Extracts of black cohosh, a plant native to North America, are marketed as a "natural" form of hormone replacement therapy (HRT) and are most commonly used to treat hot flashes and other symptoms of menopause.

Studies so far have come to conflicting conclusions about whether black cohosh works.

There have also been concerns raised about its safety. Reports of liver inflammation and liver failure in a small number of black cohosh users prompted some countries, like Australia and the UK, to require warning labels on the products.

But it has never been clear that black cohosh was to blame for those cases of liver damage. in most cases, doctors were unable to account for the patients' drinking habits or use of medications that can harm the liver.

And many postmenopausal women who are plagued by hot flashes and night sweats prefer to try black cohosh instead of taking hormones. Hormone replacement therapy, or HRT, has been controversial since 2002, when the Women's Health Initiative, a massive government-sponsored clinical trial, found that women on HRT had higher rates of heart attack, stroke, breast cancer and blood clots than placebo users.

Experts now advise that while HRT is effective for menopausal symptoms, women should take the lowest possible dose for the shortest time possible.

For the new study, reported in the journal Menopause, researchers combined the results of five previously published clinical trials of the black cohosh product Remifemin. together, the studies involved more than 1,100 women who used either this black cohosh product or a comparison substance — either an inactive placebo or a hormonal medication called tibolone — for three to six months.

Overall, the researchers found, 88 women dropped out of the studies, but none did so because of abnormal liver enzymes, a potential sign of liver damage.

And there was no evidence that black cohosh triggered harmful changes in liver enzymes. in both the black cohosh and comparison groups, about 5 percent of women developed abnormally high levels of a liver enzyme known as AST.

On the other hand, of 37 black cohosh users who had abnormally high AST levels before treatment, 62 percent saw those levels drop back into the normal range during therapy.

The study was led by Dr. Belal Naser of Salzgitter, Germany-based Schaper & Brummer GmbH & Co., which manufactures Remifemin.

But an expert not involved in the study said the findings are consistent with other evidence that black cohosh is safe for the liver.

Dr. Richard B. van Breemen, a professor at the University of Illinois College of Pharmacy in Chicago, was part of a 2009 clinical trial that tested black cohosh against a placebo, standard hormone replacement and red clover — another alternative therapy for menopause symptoms.

They found that over one year, black cohosh was no better than the placebo for easing hot flashes and night sweats.

But there was also no evidence that the herb harmed women's liver function.

"although black cohosh did not prevent hot flashes in menopausal women in our study, we found that black cohosh was safe," van Breemen told Reuters Health in an email. "in particular, we tested for liver damage in our study and found that black cohosh was not hepatotoxic (toxic to the liver)."

That trial, which was funded by the U.S. National Institutes of Health, was not included in the current analysis — which focused only on trials of Remifemin.

that narrow focus, van Breemen noted, is a weakness of the study.

still, he said, "the conclusion…that black cohosh does not cause liver damage is consistent with the results of our investigation and many other clinical trials."

in general, experts do advise that women stop using black cohosh and tell their doctor if they develop any potential signs of liver toxicity, including abdominal pain, dark urine or jaundice (yellowing of the skin and whites of the eyes).

Three months worth of Remifemin tablets costs about $30 in the U.S. — roughly the same as Premarin, a widely used hormone replacement drug.

SOURCE: bit.ly/gANnQZ Menopause, online January 11, 2011.

(HealthDay News) — here are the latest clinical trials, courtesy of ClinicalConnection.com:

Treatment Resistant Depression

This study of an investigational drug is for people who are taking an antidepressant, but still feel a lack of energy or have unresolved symptoms of depression.

The research site is in Upland, Calif.

More information

Please see clinicalconnection.com/clinical_trials/condition/depression.aspx.

Plaque Psoriasis

This study of an investigational drug is for people aged 18 to 65 diagnosed with psoriasis. the trial is for research purposes, and is not intended to treat a medical condition.

The research site is in Miramar, Fla.

More information

Please see clinicalconnection.com/clinical_trials/condition/psoriasis.aspx.

Chronic Pain

To qualify for this study, you must have chronic pain and be taking prescription pain medication.

The research site is in Dallas, Texas.

More information

Please see clinicalconnection.com/clinical_trials/condition/chronic_pain.aspx.

—–

Copyright 2011 ClinicalConnection.com. All rights reserved.

People who regularly took a low dose of aspirin for 20 years had a lower risk of colon cancer and death, a new analysis shows.

Dr. Peter Rothwell of the University of Oxford led a team that pooled the results of four clinical trials in the United Kingdom and Sweden that studied more than 14,000 people. Half were randomly assigned to take aspirin daily and half took a placebo. in a fifth trial, different doses of aspirin were compared.

After 20 years, there were 25 percent fewer colon cancer cases and 35 percent fewer deaths in the aspirin group. the benefit appeared seven to eight years after participants started taking aspirin. There was no reduction in rectal cancer cases.

Patients did not get any added benefit from taking doses over 75 milligrams per day — just under the American “baby aspirin’’ dose of 81 milligrams — and very low doses of 30 milligrams seemed to be less effective.

There were differences in where colorectal cancer developed. Aspirin use cut the risk of cancer in the upper colon by 55 percent.

BOTTOM LINE: People who took low-dose aspirin for 20 years had a reduced risk of colon cancer and death during that period.

CAUTIONS: Aspirin can cause bleeding in the digestive tract, and people seeking treatment for bleeding might have been diagnosed with colon cancer sooner than if they weren’t suffering from that side effect. That early detection could have affected mortality rates among aspirin users.

WHERE TO FIND IT: the Lancet, online Dec. 7

Cranberry remedy looks questionable many women believe drinking cranberry juice works to prevent urinary tract infections, and some scientific studies have backed them up. a new clinical trial that was larger and more rigorous than previous research found the opposite: Women who drank cranberry juice after having a urinary tract infection were no less likely to have a recurrence than women who drank a placebo.

“it is possible that the placebo juice inadvertently contained the active ingredients that reduce urinary tract infection risk, since both juices contained Vitamin C,’’ said Betsy Foxman of the University of Michigan School of Public Health. Foxman and her colleagues conducted the study.

“another possibility is that the study protocol kept participants better hydrated, leading them to urinate more frequently, therefore decreasing bacterial growth and reducing urinary tract infection symptoms.’’

BOTTOM LINE: Women who drank 8 ounces of cranberry juice twice a day after having a urinary tract infection were not less likely to have a recurrence in six months than similar women who drank juice without cranberry’s active ingredient.

CAUTIONS: Scientists are uncertain what the actual active ingredient in cranberry juice might be.

WHERE TO FIND IT: Clinical Infectious Diseases, Jan. 1

© Copyright 2010 Globe Newspaper Company.

Carolyn Dean MD ND | Tuesday, December 14, 2010

A reader just asked if there was any truth to the report that’s flooded the internet under the heading “Study Verifies that there is no value In any Flu Vaccine.”

In order to grab attention most headlines stretch the truth. This one does a bit, but the facts are still clear that flu vaccines don’t perform like the drug companies say they do.

The organization that did this review is The Cochrane Collaboration. It’s a group of over 10,000 volunteers in more than 90 countries who review the effects of health care interventions compiles data from research studies and tries to draw a conclusion based on the facts reported.

Here’s what they said. take special note of the Warning that industry studies are biased in favor of vaccination, which, to my mind, invalidates all those studies.

Main ResultsWe included 50 reports. forty (59 sub-studies) were clinical trials of over 70,000 people. Eight were comparative non-RCTs (randomized controlled trials) and assessed serious harms. Two were reports of harms which could not be introduced in the data analysis. In the relatively uncommon circumstance of vaccine matching the viral circulating strain and high circulation, 4% of unvaccinated people versus 1% of vaccinated people developed influenza symptoms. The corresponding figures for poor vaccine matching were 2% and 1%. these differences were not likely to be due to chance. Vaccination had a modest effect on time off work and had no effect on hospital admissions or complication rates. Inactivated vaccines caused local harms and an estimated 1.6 additional cases of Guillain-Barré Syndrome per million vaccinations. The harms evidence base is limited.

Authors’ ConclusionsInfluenza vaccines have a modest effect in reducing influenza symptoms and working days lost. there is no evidence that they affect complications, such as pneumonia, or transmission.

WARNING:This review includes 15 out of 36 trials funded by industry (four had no funding declaration). an earlier systematic review of 274 influenza vaccine studies published up to 2007 found industry funded studies were published in more prestigious journals and cited more than other studies independently from methodological quality and size. Studies funded from public sources were significantly less likely to report conclusions favorable to the vaccines. The review showed that reliable evidence on influenza vaccines is thin but there is evidence of widespread manipulation of conclusions and spurious notoriety of the studies. The content and conclusions of this review should be interpreted in light of this finding.

My advice? take Vitamin D this winter to prevent the flu. on Wednesday December 15, 2010 at 7pm PST. I’ll be doing my second hour-long webinar with Dr. Lani Simpson. This one is specifically on Vitamin D. to attend this free seminar, just sign up at lanisimpson.com. For those with a time challenge, I will be putting the audio portion of both webinars on my website soon.

P.S. I apologize in advance to people who write me with personal health questions. I will no longer be able to answer them but must confine myself to answering emails from clients and members of Future Health now! I am working on cloning myself and when that process is complete I will then be able to answer the 100+ emails I get every day. However, please send general questions that I may be able to answer in my blog.

Clinical trials need to be finished in an unprejudiced way, if their formula have been to be deemed reliable. Metastatic Breast Cancer Symptoms this would call for women to be incidentally reserved in to a single or some-more diagnosis groups. In a end, a outcomes of a diagnosis of a assorted groups of a hearing have been compared opposite any other. Randomization of investigate subjects in clinical trials is obliged for a most latest advances in cancer treatment. Data drawn from multiform trials have shown which rebate operation as good as deviation caring have been as in effect as some-more invasive mastectomies (breast resection). Some additionally uncover which upon condition which chemotherapy to women with non-metastasized breast cancer prevents a entrance of systemic widespread as good as which a operate of tamoxifen (a resourceful estrogen receptor modulator) increases a heal rate in women with hormone certain breast cancer. through a randomized method, a medicine as good as questioner disposition has been eliminated, which is a vital complaint in clinical investigate trials comparing a novel caring to customary treatment.

Women who have been peaceful to experience in clinical investigate trials have finished a poignant grant to healing advancement. Each of these trials tests a latest supposition as good as a formula afterwards turn a believe bottom for next clinical trials. In sequence to uncover poignant differences in healing modalities, multiform thousand women have been indispensable as investigate subjects for any trial. These volunteers have been good wakeful which they might be removing determined or initial diagnosis as good as will not be told which. These women bravely participated with this bulk of uncertainty, not meaningful if a single diagnosis is some-more or rebate in effect than a other, though concluded to assistance answer a subject of which a some-more optimal caring was. The disproportion in any diagnosis fast in trials currently involves a sequencing of assorted treatments or a further of a latest drug.

There have been additionally studies called commander trials. These have been customarily finished in a core which is implementing clinical investigate which is not sponsored by a National Cancer Institute as good as is not randomized. usually, these studies have been sponsored by drug companies, or conducted during a university. there have been safeguards in place in commander studies to strengthen a investigate subjects as most as possible. Oftentimes, these protocols have been usually for women with modernized cancer who might be peaceful to place themselves during risk since of singular diagnosis options accessible to them during which which late theatre of breast cancer.

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Most tellurian clinical investigate trials have been widely separated in to 3 phases depending upon a question, which it is attempting to answer. Phase we contrast is written to establish if a latest diagnosis has excusable tolerability to cancer patients as good as during what dose poignant side goods begin to occur. Once a drug or a diagnosis process has been proven safe, Phase II clinical trials quantifies a design reply rate, which is, if diagnosis formula in a quantifiable rebate in cancer. In women with breast cancer, both Phase we as good as II contrast is achieved upon those with metastatic spread. Phase III contrast involves a more aged of customary diagnosis to a earnest a single which has already left by Phase we as good as II testing. most women enrolled in this proviso of clinical trials have been those with a newly diagnosed breast cancer.

If we have breast cancer as good as we would instruct to experience in such a trial, ask your oncologist if we have been authorised to enroll in one. Your capability to experience might rely upon a illness caring smoothness complement we have been in, so we should speak to your Health Insurance Company or HMO representative. Generally, a entrance years should infer really earnest in a margin of breast cancer research, essentially since there have been unusual systematic resources being dedicated to a cause.

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